Similar Rate-pressure Product Research Articles

Sex differences of sequential changes in coronary blood flow and microvascular function in patients with suspected angina.

This study evaluated the sex differences of sequential changes in coronary blood flows and microvascular function in patients with suspected angina but with no obstructed coronary arteries. A total of 202 consecutive patients who experienced chest pain but had no significant coronary artery stenosis and who underwent adenosine stress echocardiography were included in the study. Coronary blood flow (CBF) velocities were measured at 1, 2, and 3min after adenosine infusion. The mean age was 61years, and 138 (68%) were women. Approximately 40% of patients had coronary microvascular dysfunction (CMD, coronary flow velocity reserve < 2.3), with women exhibiting higher CMD prevalence. The left ventricular (LV) mass index was similar between men and women, while women exhibited higher baseline rate pressure products (RPP). At baseline, coronary blood flow velocities were similar between the sexes. However, CBF velocities in women gradually increased during the examination; and in men, the increase was abrupt and steep during the early stages of examination (p = 0.015 for interaction between time and sex), even with similar RPP in stress. Coronary flow velocity reserve was steadily lower in women compared to men (1min, 2.09 ± 0.86 vs 2.44 ± 0.87; 2min, 2.39 ± 0.72 vs 2.63 ± 0.85; 3min, 2.45 ± 0.70 vs 2.68 ± 0.73). In patients with suspected angina but with no obstructed coronary arteries, CMD was especially prevalent among women. Women exhibited higher oxygen consumption, while exhibiting slower and gradual increases in CBF velocities. Conversely, men exhibited faster and steeper increases in CBF velocities even with similar RPP in stress.

Head-to-Head Comparison of Peak Supine Bicycle Exercise Echocardiography and Treadmill Exercise Echocardiography at Peak and at Post-Exercise for the Detection of Coronary Artery Disease

Supine bicycle exercise (SBE) echocardiography and treadmill exercise (TME) echocardiography have been used for evaluation of coronary artery disease (CAD). Although peak imaging acquisition has been considered unfeasible with TME, higher sensitivity for the detection of CAD has been recently found with this method compared with post-TME echocardiography. However, peak TME echocardiography has not been previously compared with the more standardized peak SBE echocardiography. The aim of this study was to compare peak TME echocardiography, peak SBE echocardiography, and post-TME echocardiography for the detection of CAD. A series of 116 patients (mean age, 61 ± 10 years) referred for evaluation of CAD underwent SBE (starting at 25 W, with 25-W increments every 2-3 min) and TME with peak and postexercise imaging acquisition, in a random sequence. Digitized images at baseline, at peak TME, after TME, and at peak SBE were interpreted in a random and blinded fashion. All patients underwent coronary angiography. Maximal heart rate was higher during TME, whereas systolic blood pressure was higher during SBE, resulting in similar rate-pressure products. On quantitative angiography, 75 patients had coronary stenosis (≥50%). In these patients, wall motion score indexes at maximal exercise were higher at peak TME (median, 1.45; interquartile range [IQR], 1.13-1.75) than at peak SBE (median, 1.25; IQR, 1.0-1.56) or after TME (median, 1.13; IQR, 1.0-1.38) (P= .002 between peak TME and peak SBE imaging, P < .001 between post-TME imaging and the other modalities). The extent of myocardial ischemia (number of ischemic segments) was also higher during peak TME (median, 5; IQR, 2-12) compared with peak SBE (median, 3; IQR, 0-8) or after TME (median, 2; IQR, 0-4) (P < .001 between peak TME and peak SBE imaging, P < .001 between post-TME imaging and the other modalities). ST-segment changes in patients with CAD and normal baseline ST segments were higher during TME (median, 1 mm [IQR, 0-1.9 mm] vs 0 mm [IQR, 0-1.5 mm]; P= .006). The sensitivity of peak TME, peak SBE, and post-TME echocardiography for CAD was 84%, 75%, and 60% (P= .001 between post-TME and peak TME echocardiography, P= .055 between post-TME and peak SBE echocardiography), with specificity of 63%, 80%, and 78%, respectively (P= NS) and accuracy of 77%, 77%, and 66%, respectively (P= NS). Peak TME echocardiography diagnosed multivessel disease in 27 of the 40 patients with stenoses in more than one coronary artery, in contrast to 17 patients with peak SBE imaging and 12 with post-TME imaging (P < .05 between peak TME imaging and the other modalities). Image quality was similar with the three techniques. The duration of the test was longer with SBE echocardiography (9.5 ± 3.8 vs 7.6 ± 2.5 min, P < .001). During TME and SBE, patients achieve similar double products. Ischemia is more extensive and frequent with peak TME, which makes peak TME a more valuable exercise echocardiographic modality to increase sensitivity. However, peak SBE should be preferred to TME if the latter is performed with postexercise imaging acquisition.

Effects of perhexiline on myocardial deformation in patients with ischaemic left ventricular dysfunction

BackgroundPerhexiline improves functional capacity in heart failure, but the mechanisms are undefined. We sought its effects on myocardial deformation in patients with viable myocardium. MethodsThirty-six medically-treated patients, stable at least 6 months post-infarction with LV dysfunction and myocardial viability shown by dobutamine echo (DbE) were randomised to receive perhexiline or matching placebo for 1 year. Cardiopulmonary exercise testing and DbE were performed at baseline and follow-up. Peak-systolic strain (S) and strain rate (SR) were measured offline in 111 dysfunctional segments in the placebo and 88 in the treatment group at rest, low-dose (LDD) and peak-dose dobutamine (PDD). ResultsThe serum perhexiline level was 0.27±0.7 µg/l. There was no difference in the wall motion response to dobutamine at baseline and follow-up. Resting strain and SR were similar in the two groups at baseline and follow-up. However, SR at LDD and PDD increased in the placebo group and worsened during the same period in the perhexiline group. Patients on perhexiline and placebo had a similar rate-pressure product and exercise duration at baseline (7.9±2.7 vs 8.7±3.3 min, p=NS) and follow-up (9.6±4.6 vs 10.1±3.03 min, p=NS). ConclusionPerhexiline does not improve the deformation of abnormal myocardial segments in patients with ischaemic LV dysfunction.

Stress testing response in women heterozygous for familial hypercholesterolemia

We evaluated 62 exercise treadmill tests (ETTs) in equal numbers of heterozygous for familial hypercholesterolemia (hFH) and healthy (HLY) women, matched for age, baseline systolic and diastolic blood pressure (BP) and baseline heart rate (HR), using the Bruce protocol. Both groups had similar rate pressure product (RPP) and workload in metabolic equivalents (METs) (27,563 ± 3124 vs. 29,090 ± 4077, p = 0.103 and 11.2 ± 1.7 vs. 11.5 ± 1.8, p = 0.473, respectively). Women with hFH had lower delta (difference of peak to baseline) and peak exercise systolic and diastolic BP (systolic: 48 ± 12 vs. 58 ± 17 mmHg, p = 0.010 and 167 ± 19 vs. 177 ± 17 mmHg, p = 0.042, respectively; diastolic: 11 ± 7 vs. 15 ± 7 mmHg, p = 0.028 and 85 ± 7 vs. 91 ± 7 mmHg, p < 0.001, respectively). Furthermore, women with hFH had higher delta percentage (%) of HR, compared to HLY; (106 ± 25 vs. 95 ± 20, p = 0.047). In conclusion, hFH women possibly have an inadequate rise in systolic BP during ETT. Diastolic BP increased more in the HLY than in the hFH group, but still remained within normal limits. These findings may reflect preclinical changes of atherosclerosis in hFH women, however further research should be undertaken.

Coronary microvascular adaptation to myocardial metabolic demand can be restored by inhibition of iron-catalyzed formation of oxygen free radicals in type 2 diabetic patients.

Dilation of coronary vessels is impaired in diabetic patients when myocardial metabolic demand is increased. Deferoxamine (DFX) restores a normal dilation of epicardial coronary arteries. To assess the effects of DFX on metabolic coronary microvascular dilation in type 2 diabetic patients, coronary blood flow was measured using intracoronary Doppler and quantitative angiography in 17 type 2 diabetic patients with normal coronary arteries and without any other coronary risk factors. Measurements were made at baseline and during a cold pressor test (CPT), before and after intravenous administration of DFX. With a similar rate-pressure product (RPP) increase during CPT before and after DFX (+21.1 +/- 8.7 vs. +20.5 +/- 8.9%, respectively), coronary blood flow increase was significantly enhanced after DFX (+31.8 +/- 16.7 vs. +6.3 +/- 12.9% before DFX, P < 0.001). Moreover, coronary resistance increased during CPT before DFX and decreased after DFX (+14.8 +/- 21.9 vs. -7.9 +/- 10.9%, respectively, P < 0.001). Lastly, the negative relationship between coronary blood flow and RPP before DFX (R = 0.546, P < 0.05) was changed in a positive relationship after DFX (R = 0.518, P < 0.05). In conclusion, in type 2 diabetic patients, inhibition of iron-catalyzed oxidative reactions by DFX restored dilation of the coronary microcirculation and a normal matching between myocardial metabolic demand and coronary blood flow.

Hyperventilation test in syndrome X.

The hyperventilation (HV) test has been extensively used in different forms of coronary artery disease. The purpose of this work was to investigate the response to HV in patients with syndrome X and compare HV with exercise (EX) test. The authors studied 20 patients with syndrome X (angina, a positive EX test, and normal coronary angiogram) and 20 healthy subjects who underwent HV and EX tests. In 7 patients, all women, angina and electrocardiographic (ECG) changes occurred during HV but in none of the controls. Patients with syndrome X and controls had a similar rate-pressure product (RPP) at rest and achieved a similar RPP with HV. The RPP achieved with HV in patients with syndrome X without ECG changes was significantly lower, 121.8 +/-29.1(mean +/-SD), than what was achieved by those with changes, 167.9 +/-42.9, P < 0.01. In patients with an abnormal response to HV the RPP at which angina and ECG changes occurred was similar to that where similar changes were observed during EX. There was a significant correlation of the RPPs between the two tests, r=0.82, P < 0.02. In contrast, in patients in whom no angina or ECG changes occurred, the RPP they achieved with HV was significantly lower than the anginal threshold during EX 204 +/- 47.4, P < 0.0001. In conclusion, a significant proportion of patients with syndrome X, mainly women, who achieve a high RPP with HV, develop angina and ECG changes during overbreathing. The close relation between EX and HV RPPs where these changes occur suggests an increased myocardial oxygen demand as the most likely underlying mechanism for this behavior.

Global alteration in perfusion response to increasing oxygen consumption in patients with single-vessel coronary artery disease.

Recent evidence suggests that, in coronary artery disease (CAD), myocardial blood flow (MBF) regulation is abnormal in regions supplied by apparently normal coronary arteries. However, the relation between this alteration and MBF response to increasing metabolic demand has not been fully elucidated. MBF was assessed at baseline, during atrial pacing tachycardia, and after dipyridamole (0.56 mg/kg IV over 4 minutes) in 9 normal subjects and in 24 patients with ischemia on effort, no myocardial infarction, and isolated left anterior descending (n = 19) or left circumflex (n = 5) coronary artery stenosis (> or = 50% diameter narrowing). Perfusion of both poststenotic (S) and normally supplied (N) areas was measured off therapy by positron emission tomography and [13N]ammonia. Normal subjects and CAD patients showed similar rate-pressure products at baseline, during pacing, and after dipyridamole. In CAD patients, MBF was lower in S than in N territories at rest (0.68 +/- 0.14 versus 0.74 +/- 0.18 mL.min-1.g-1, respectively, P < .05), during pacing (0.92 +/- 0.29 versus 1.16 +/- 0.40 mL.min-1.g-1, respectively, P < .01), and after dipyridamole (1.18 +/- 0.34 versus 1.77 +/- 0.71 mL.min-1.g-1, respectively, P < .01). However, normal subjects showed significantly higher values of MBF both at rest (0.92 +/- 0.13 mL.min-1.g-1, P < .05 versus both S and N areas), during pacing tachycardia (1.95 +/- 0.64 mL.min-1.g-1, P < .01 versus both S and N areas), and after dipyridamole (3.59 +/- 0.71 mL.min-1.g-1, P < .01 versus both S and N areas). The percent change in flow was strictly correlated with the corresponding change in rate-pressure product in normal subjects (r = .85, P < .01) but not in either S (r = .04, P = NS) or N regions (r = .08, P = NS) of CAD patients. Besides epicardial stenosis, further factors may affect flow response to increasing metabolic demand and coronary reserve in patients with CAD.

Epidural spinal electrical stimulation for severe angina: a study of its effects on symptoms, exercise tolerance and degree of ischaemia

The effectiveness of epidural spinal electrical stimulation has been studied in 14 patients with severe intractable angina unresponsive to standard therapies including bypass grafting. After implantation of the neurostimulator units the patients were assessed by a symptom questionnaire, treadmill exercise testing and right atrial pacing. There was a significant improvement of symptoms and GTN consumption fell markedly. With the neurostimulator on, exercise duration increased from a mean (CI) of 414 (153) to 478 (149) s, and total ST segment depression was less both at maximum exercise (7.1 (4.5) vs 5.6 (4.2) mm) and at 90% of the maximum control heart rate (3.5 (3.7) vs 2.6 (4.3) mm), with similar rate-pressure product at maximum exercise. With right atrial pacing the maximum heart rate reached before onset of angina was increased (143 (14) to 150 (7) b.min-1) and total ST segment depression was less at all heart rates. Benefit has persisted in some patients for over 2 years without any apparent adverse sequelae. Epidural spinal electrical stimulation is, therefore, an alternative therapy for some patients with intractable angina which has not responded to standard therapies.

Quantification of absolute myocardial perfusion at rest and during exercise with positron emission tomography after human cardiac transplantation

The maximal exercise capacity of cardiac transplant recipients is reduced compared with that of normal subjects. To determine if this reduced exercise capacity is related to inadequate myocardial perfusion during exercise, myocardial perfusion was measured noninvasively with use of positron emission tomography and nitrogen (N)-13 ammonia. Twelve transplant recipients with no angiographic evidence of accelerated coronary atherosclerosis were studied. Serial N-13 ammonia imaging was performed at rest and during supine bicycle exercise. The results were compared with those from 10 normal volunteers with a low probability of having cardiac disease. A two-compartment kinetic model for estimating myocardial perfusion was applied to the data.Transplant recipients achieved a significantly lower exercise work load than did the volunteers (42 ± 16 vs. 128 ± 22 W), but a higher venous lactate concentration (31.3 ± 14.9 vs. 13.7 ±4.1 mg/100 ml). Despite the difference in exercise work load, there was no significant difference in the cardiac work achieved by transplant recipients and normal subjects as evidenced by similar rate-pressure products of 24,000 ± 3,400 versus 21,300 ±2,800 beats/min per mm Hg, respectively. In addition, myocardial blood flow during exercise was not significantly different between the two groups (1.70 ± 0.60 vs. 1.56 ± 0.71 ml/min per g, respectively).This study demonstrates that the myocardial flow response to the physiologic stress of exercise is appropriate in transplant recipients and does not appear to explain the decreased exercise capacity in these patients.

Relation between the O2 supply:demand ratio, , and adenosine formation in hearts stimulated with inotropic agents

Mooted controllers of adenosine formation in heart are the oxygen supply:demand ratio, myocardial oxygen consumption (MVO2), the cytosolic phosphorylation potential (log[ATP]/[ADP][Pi]). The relationship between these parameters and purine release (adenosine + inosine) into the venous effluent was examined in isovolumic rat hearts perfused at 20 and 12 mL.min-1.g-1 with a glucose containing crystalloid buffer and stimulated with inotropic agents (isoproterenol, norepinephrine, 3-isobutyl-1-methylxanthine, and ouabain). The oxygen supply:demand ratio and MVO2 were continuously determined using an oxygen electrode to monitor oxygen supply and consumption. The phosphorylation potential was calculated from phosphorus metabolite levels determined by 31P-NMR spectroscopy and HPLC analysis. Left ventricular function was assessed as the rate-pressure product. All inotropic agents increased the rate-pressure product, with increases in function being greater in the hearts perfused at 20 mL.min-1.g-1. MVO2 was linearly related to the rate-pressure product at each flow rate; however, the hearts perfused at 20 mL.min-1.g-1 exhibited approximately twofold greater MVO2 values for similar rate-pressure product values. All inotropic agents increased adenosine release into the venous effluent. While there was a significant linear relation between adenosine formation and MVO2 in hearts perfused at both flow rates and stimulated with drugs, the relations differed with adenosine release being approximately fourfold greater in hearts perfused at 12 mL.min-1.g-1 under similar conditions of MVO2. Adenosine formation correlated exponentially with the ratio of oxygen supply:demand under all conditions (r = 0.97) and the relation did not differ significantly between hearts perfused at different rates.(ABSTRACT TRUNCATED AT 250 WORDS)

Comparison of ST segment depression in upright treadmill and supine bicycle exercise testing

Significant differences in the hemodynamic response to upright and supine exercise have been reported in patients with coronary artery disease. The purpose of the present study was to compare the degree of myocardial ischemia as assessed by ST segment depression during upright treadmill and supine bicycle exercise in 98 patients with coronary artery disease and in 34 patients with normal coronary arteries. The amount of ST segment depression at maximal exercise in patients with coronary artery disease was 0.90 ± 0.80 mm for treadmill and 1.34 ± 1.09 mm for supine bicycle (p < 0.001). The amount of ST segment depression during treadmill and supine bicycle exercise tests was also compared at highest similar heart rates (0.68 ± 0.77 versus 1.17 ± 1.01, p < 0.001), at highest similar rate-pressure products (0.71 ± 0.77 versus 1.08 ± 1.04, p < 0.001), at highest similar metabolic equivalents of oxygen consumption (MET) levels (0.69 ± 0.75 versus 1.20 ± 1.05 mm, p < 0.001) and at the onset of angina (0.84 ± 0.73 versus 1.18 ± 0.88 mm, p < 0.001). The rate-pressure product achieved at maximal exercise was similar in both tests (18.74 ± 5.80 × 103versus 18.81 ± 5.17 × 103, p = NS). The occurrence of angina during treadmill and supine bicycle exercise tests was similar (47 of 98 versus 48 of 98, respectively, p = NS). For the detection of coronary artery disease, the sensitivity was 50.0% for treadmill and 63.3% for supine bicycle (p < 0.05) and the specificity was 73.5 versus 70.6%, respectively (p = NS).Thus, the degree of ST segment depression in patients with coronary artery disease is significantly greater during supine bicycle exercise than during upright treadmill testing at the onset of angina, at similar rate-pressure products, at similar heart rates, at similar MET levels and at maximal exercise. Supine bicycle exercise electrocardiography is significantly more sensitive, yet equally specific for the dejection of coronary artery disease when compared with upright treadmill exercise electrocardiography.

Comparison of determinants of myocardial oxygen consumption during arm and leg exercise in normal persons

Arm exercise assumes an increasingly important role in clinical cardiology as it is used in both exercise testing and training of patients with coronary artery disease. The effects of arm exercise on myocardial oxygen consumption are not well understood; they may differ from the effects of leg exercise. Previous studies have shown that the ischemic threshold is higher in patients performing arm exercise and leg exercise at the same heart rate-blood pressure product. The contribution of other determinants of myocardial oxygen consumption—left ventricular (LV) peak meridional systolic wall stress and contractility—to these observed differences were studied. Thirty healthy subjects exercised to the same peak rate-pressure product during dynamic upper- and lower-extremity exercise. Peak workload was lower during arm exercise (100 ± 16 W) than during leg exercise (170 ± 21 W, p < 0.001). LV wall stress did not differ during either form of exercise (197 ± 44 vs 204 ± 33 dynes/cm 2 × 10 3, arm vs leg, respectively). This was also true of contractility as assessed by the velocity of circumferential fiber shortening (2.8 ± 0.6 vs 2.5 ± 0.4 circ/s, arm vs leg, respectively) and the preejection period/LV ejection time ratio (0.33 ± 0.11 vs 0.31 ± 0.07, arm vs leg, respectively). Normal subjects exercising to a similar rate-pressure product showed the same levels of LV wall stress and contractility for arm and leg exercise despite the lower workload performed with arm exercise.

Silent myocardial ischemia: Hemodynamic changes during dynamic exercise in patients with proven coronary artery disease despite absence of angina pectoris

The hemodynamic changes during exercise occurring in 36 patients with proven coronary artery disease (10 without and 26 with previous myocardial infarction) who tolerated the stress test without angina were analyzed and compared with changes observed in a control group of 36 carefully matched patients whose exercise was limited by angina. All patients were exercised to the same extent, reaching a similar rate-pressure product at the end of the stress test (19,508 +/- 4,828 [SD] versus 19,247 +/- 4,117 beats/min X mm Hg [NS] in the study and control groups without prior infarction, and 19,665 +/- 3,950 versus 17,701 +/- 4,600 beats/min X mm Hg [NS] in the respective groups with infarction). In all groups left ventricular end-diastolic pressure increased from rest to exercise (from 18 +/- 4 to 36 +/- 11 and from 13 +/- 5 to 29 +/- 9 mm Hg, respectively, in the study and control groups without prior infarction and from 17 +/- 7 to 32 +/- 13 and from 19 +/- 7 to 36 +/- 9 mm Hg in the respective groups with prior infarction). Left ventricular ejection fraction decreased (from 59 +/- 7 to 50 +/- 15 and from 60 +/- 4 to 52 +/- 9% in the study and control groups without prior infarction and from 54 +/- 9 to 47 +/- 10 and 55 +/- 9 to 50 +/- 4% in the respective groups with prior infarction). Whereas the changes from rest to exercise were highly significant within each group, no significant differences were noted between the corresponding groups. Regional de novo hypokinesia appeared in all patients without prior infarction and in 25 and 22 patients, respectively, of the groups with prior infarction. Thus, under similar physical stress conditions, comparable hemodynamic changes indicative of ischemia are observed in patients with significant coronary artery lesions with or without previous myocardial infarction irrespective of the occurrence of angina. Therefore, angina pectoris cannot be considered a prerequisite for hemodynamically significant ischemia during exertion.

Treatment of stable angina of effort with verapamil: a double-blind, placebo-controlled randomized crossover study.

The effects of verapamil were assessed in 26 patients with stable exertional angina pectoris in a double-blind, placebo-controlled, randomized crossover protocol using serial treadmill tests. Verapamil, 480 mg/day, reduced anginal frequency from 5.6 +/- 7.3 to 2.2 +/- 3.9 attacks per week (p less than 0.001) and nitroglycerin consumption from 3.4 +/- 4.9 to 1.2 +/- 2.5 tablets per week (p less than 0.05) compared with placebo. Treadmill time increased from 6.4 +/- 2.1 minutes during the placebo phase to 7.5 +/- 1.8 minutes during the verapamil phase (p less than 0.001). Verapamil's beneficial effect appeared to be related, in part, to a 10% reduction of the rate-pressure product at rest (p less than 0.05) and a 12% reduction during submaximal exercise (p less than 0.001). Verapamil also caused less marked ST-segment depressions at peak exercise (p less than 0.05) at a similar rate-pressure product, suggesting a favorable redistribution of coronary blood flow to the ischemic zone. Side effects from verapamil were minimal, consisting mainly of constipation (six patients). Verapamil appears to be a safe and effective drug for treating angina of effort.

Decreased frequency of exercise-induced ventricular ectopic activity in the second of two consecutive treadmill tests.

Two exercise tests were performed with an intervening rest period of 45 minutes in a group of 13 subjects with previously identified exercise-induced ventricular arrhythmias and no resting arrhythmias. Both normal subjects and patients with heart disease were included in the group. The level of stresss was equal in both tests as judged by similar rate-pressure products at peak exercise. There was a significant decrease (P less than 0.05) in the number of VPCs induced by exercise during and after the second test. When the number of VPCs on test I and test II in the same patients were compared, a regression line fitted the data well (r = 0.92). Analysis of the recovery periods revealed significant (P less than 0.01) decreases in systolic blood pressure at one and three minutes post exercise, comparing the second to the first test. The underlying mechanism may be decreased myocardial oxygen demand during the second test as the lowered rate-pressure products during recovery (P less than 0.01) reflect. The results of this study indicate that tests of effectiveness of an antiarrhythmic drug should not be based solely on a decrease in the amount of severity of ventricular irritability between two successive exercise tests, one immediately before and the other following administration of the drug.